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HOME > Cancer Res Treat > Volume 57(2); 2025 > Article
Original Article
Hematologic malignancy The Role of Direct Oral Anticoagulants in Managing Myeloproliferative Neoplasms Patients
Ji Yun Leeorcid, Ju-Hyun Lee, Woochan Park, Jeongmin Seo, Minsu Kang, Eun Hee Jung, Sang-A Kim, Koung Jin Suh, Ji-Won Kim, Se Hyun Kim, Jeong-Ok Lee, Jin Won Kim, Yu Jung Kim, Keun-Wook Lee, Jee Hyun Kim, Soo-Mee Bangorcid
Cancer Research and Treatment : Official Journal of Korean Cancer Association 2025;57(2):612-620.
DOI: https://doi.org/10.4143/crt.2024.738
Published online: September 20, 2024

Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea

Correspondence: Soo-Mee Bang, Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Gumi-ro 173 Beon-gil, Bundang-gu, Seongnam 13620, Korea
Tel: 82-31-787-7039 E-mail: smbang7@snu.ac.kr
• Received: August 5, 2024   • Accepted: September 19, 2024

Copyright © 2025 by the Korean Cancer Association

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Purpose
    Thrombosis and bleeding significantly affect morbidity and mortality in myeloproliferative neoplasms (MPNs). The efficacy and safety of direct oral anticoagulants (DOACs) in MPN patients remain uncertain.
  • Materials and Methods
    We conducted a large, retrospective, nationwide cohort study using the Korean Health Insurance Review and Assessment Service database from 2010 to 2021.
  • Results
    Out of the 368 MPN patients included in the final analysis, 62.8% were treated with DOACs for atrial fibrillation (AF), and 37.2% for venous thromboembolism (VTE). The AF group was statistically older with higher CHA2DS2-VASc (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category [female]) scores compared to the VTE group. Antiplatelet agents were used in 51.1% of cases, and cytoreductive drugs in 79.3%, with hydroxyurea being the most common (64.9%). The median follow-up was 22.3 months, with 1-year cumulative incidence rates of thrombosis and bleeding at 11.1% and 3.7%, respectively. Multivariate analysis identified CHA2DS2-VASc scores ≥ 3 (hazard ratio [HR], 3.48), concomitant antiplatelet use (HR, 2.57), and cytoreduction (HR, 2.20) as significant thrombosis risk factors but found no significant predictors for major bleeding.
  • Conclusion
    Despite the limitations of retrospective data, DOAC treatment in MPN patients seems effective and has an acceptable bleeding risk.
  • Key words: Myeloproliferative neoplasms, Direct oral anticoagulants, Thrombosis, Hemorrhage
Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs), which include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (MF), are chronic hematopoietic disorders defined by an excessive production of mature myeloid blood cells [1]. Venous and arterial thrombosis is a primary cause of morbidity and mortality due to a marked prothrombotic condition [2,3]. Compared to the general population, MPN patients have a threefold and tenfold higher rate of arterial and venous thrombosis, respectively [4]. At diagnosis, over 20.0% of MPN patients had experienced thrombosis, with arterial and venous thromboses accounting for 16.2% and 6.2% of cases, respectively [5]. During follow-up, the predicted cumulative rates of arterial thrombosis were 5.5%, 1% to 3%, and 1.75% per patient-year for PV, ET, and MF, respectively [6-8]. The estimated cumulative rates of venous thrombosis during follow-up were 1.05%, 0.6%, and 0.76% per patient-year for PV, ET, and MF, respectively [8-10]. MPNs are associated with an increased risk of bleeding [11]. Among newly diagnosed MPN patients, the pooled prevalence of hemorrhagic sequelae was 6.2%, with rates of 6.9%, 7.3%, and 8.9% in PV, ET, and MF, respectively [5]. Gastrointestinal, mucosal, and cutaneous bleeding were all common [5].
The choice of the course and duration of antithrombotic therapy in MPN patients is particularly challenging due to limited data. Major guidelines favor the use of direct oral anticoagulants (DOACs) as first-line therapies to prevent stroke or systemic embolism associated with atrial fibrillation (AF) [12,13]. DOACs are also the first-choice treatment for acute venous thromboembolism (VTE) in the general population and in cancer patients without gastrointestinal (GI) tumor [14]. In the general population, DOACs have been shown to be at least as effective as vitamin K antagonist (VKA), but with a lower rate of major bleeding complications. Given their propensity for thrombotic and hemorrhagic complications, MPN patients might benefit from reduced bleeding risks when using DOACs compared to VKAs. There are no randomized controlled trials comparing VKAs and DOACs in MPN patients; only a handful of retrospective studies exist, leaving the safety and efficacy of DOACs in this population uncertain. How et al. [15] reported that the 1-year cumulative incidence of thrombosis and bleeding on DOACs in MPN patients was 5.5% and 12.3%, respectively. According to the MPN-DOACs study, over a median follow-up period of 1.7 years, there was a 7.2% recurrence of thrombosis and a 5.9% incidence of major hemorrhagic complications on DOACs [16]. DOACs and VKAs appear to have a substantially similar risk-benefit profile in MPN, but this interpretation is based on very limited data. Therefore, this study aimed to conduct a large cohort study using a national healthcare database to examine the incidence and risk factors for thrombotic and bleeding complications in MPN patients with AF and VTE who are treated with DOACs in real-world clinical settings.
1. Data source
The Health Insurance Review and Assessment Service (HIRA) is a government-affiliated organization that has received claims from all medical institutions in Korea since 2000 [17]. The databases include demographic data, diagnoses, procedures, and prescription information from the inpatient and outpatient care of over 50 million Koreans. Diagnoses were codified according to the sixth and seventh revisions of the Korean Classification of Disease, derived from the International Classification of Disease, 10th revision (ICD-10).
2. Study population
We collected data on patients diagnosed with MPNs using diagnostic codes from January 2010 to December 2021. The selection criteria included: (1) patients newly diagnosed with one of three MPN types—PV, ET, or MF; and (2) those who were treated with one of the DOACs—rivaroxaban, apixaban, dabigatran, or edoxaban—for at least 7 days for either AF or VTE.
To ensure data accuracy, we excluded patients diagnosed before January 1, 2011, or after January 1, 2021, to account for washout periods. We also removed patients with overlapping MPN diagnostic codes, those diagnosed with end-stage renal disease, those prescribed DOACs for indications other than AF or VTE, and those with DOAC prescriptions coded concurrently for both AF and VTE. A more detailed explanation of these exclusions is available in S1 Fig. The index date for our study is defined as the date on which a patient first received a DOAC prescription during the study period.
3. Study outcomes
We observed thrombosis and bleeding outcomes during DOAC treatment. Thrombosis outcomes include arterial and venous thrombosis. Arterial thrombosis comprises ischemic stroke, transient ischemic attack, acute myocardial infarction, and peripheral arterial occlusions. Venous thrombosis encompasses lower extremity deep vein thrombosis (DVT), pulmonary embolism (PE), hepatic vein thrombosis, portal vein thrombosis, mesenteric vein thrombosis, and cerebral vein thrombosis. To define a case of thrombosis incidence, we classified patients who visited the emergency room or were hospitalized with arterial and/or venous thrombosis codes and underwent imaging as having experienced thrombosis. Bleeding outcomes include intracranial hemorrhage (ICH), hospitalizations for GI bleeding, and major bleeding, with detailed definitions described in S2 Table. We examined DOACs administered within 30 days before the clinical outcomes to assess the effects associated with their usage. Events where DOACs were not administered within 30 days prior were excluded from our analysis. Additionally, we analyzed the use of antiplatelet agents within 30 days prior to the events to determine how DOACs influence outcomes related to these agents.
4. Covariates
Comorbidities were included in the model as CHA2DS2-VASc (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category [female]) scores, assigning 1 point each for age 65-74 years, female sex, hypertension, diabetes, congestive heart failure, and vascular disease, and 2 points each for age 75 years or older, and a history of stroke, transient ischemic attack, or systemic thromboembolism [18]. Patients were classified into two groups based on their CHA2DS2-VASc scores: 0-2 and ≥ 3.
5. Statistics
Categorical data were presented as frequencies and analyzed using the chi-square test. Continuous variables were compared using the Mann-Whitney U test, with overall medians and interquartile ranges (IQRs) calculated. The duration from the initiation of DOAC therapy to the occurrence of a thrombotic or bleeding event was measured in months. A competing risks model was employed, where the primary events were thrombosis or bleeding during DOAC treatment, and the competing event was death during the treatment period. This scenario was depicted using cumulative incidence functions to estimate the risk of an event over time. Differences in cumulative incidence across patient groups were assessed using Gray’s test. Univariate and multivariate Fine-Gray regression models were used to identify potential risk factors for thrombotic or bleeding events. The 95% confidence intervals (95% CIs) for the effect sizes of each independent variable were calculated. A two-sided p-value of ≤ 0.05 was considered statistically significant. All statistical analyses were conducted using SAS Enterprise Guide 6.1 (SAS Institute Inc.).
1. Patient characteristics
The present study included 567 patients with MPN who were newly administered DOACs for AF or VTE during an 11-year period (S1 Fig.). Out of the 368 MPN patients included in the final analysis, 231 (62.8%) were treated with DOACs for AF, and 137 (37.2%) for VTE. Clinical baseline characteristics of the study cohort are shown in Table 1. Patients treated with DOACs for AF had a statistically significant higher median age, exceeding that of patients treated for VTE by 2 years (75 years vs. 73 years, p=0.048). Additionally, the prevalence of elderly patients aged 75 and older was significantly greater in the AF cohort compared to the VTE cohort (51.9% vs. 42.3%, p=0.007). Regarding sex distribution, the proportion of males was significantly higher in the AF group than in the VTE group (58.9% vs. 43.8%, p=0.005).
Among the MPN subtypes, ET was the most prevalent (48.6%), followed by PV (32.3%), and MF (19.0%). There was a trend in MPN subtype distribution between the AF and VTE groups, especially with a notable difference in the proportion of MF (15.6% vs. 24.8%, p=0.041). Overall, the CHA2DS2-VASc score was statistically significantly higher in the AF group compared to the VTE group. Additionally, the prevalence of hypertension and congestive heart failure was significantly greater in the AF group than in the VTE group (p < 0.001 for both conditions). Among the DOACs, rivaroxaban was the most used (37.2%), followed by apixaban (30.7%), edoxaban (24.5%), and dabigatran (7.6%). More than half of the patients (51.1%) were on antiplatelet therapy, with aspirin being the most common (44.6%), followed by clopidogrel (23.1%). Furthermore, 79.3% of the patients received cytoreductive therapy, with hydroxyurea being the most frequently used (64.9%), followed by anagrelide (27.4%) and ruxolitinib (12.2%). Hydroxyurea was the most used agent in both groups, whereas anagrelide was more frequently used in the AF group compared to the VTE group (31.2% vs. 21.2%, p=0.038). Conversely, ruxolitinib was more commonly used in the VTE group than in the AF group (17.5% vs. 9.1%, p=0.017). In MPN patients treated with DOACs for VTE, the most prevalent subtype was DVT (37.2%), followed by PE alone (34.3%), unusual site VTE (16.8%), and DVT combined with PE (11.7%) (S3 Table).
2. Incidence of thrombosis
The median follow-up for all patients was 22.3 months (IQR, 7.1 to 44.1). In our cohort, 45 patients (12.2%) experienced thrombotic events on DOACs, including 29 (7.9%) with arterial thrombosis and 20 (5.4%) with venous thrombosis. The 1-year cumulative incidence of thrombosis on DOACs was 11.1% (95% CI, 7.7 to 15.2) (Fig. 1A).
The median follow-up for the AF cohort was 24.7 months (IQR, 7.8 to 46.3). In this cohort, 30 patients (13.0%) experienced thrombotic events, including 22 (9.5%) with arterial thrombosis and 10 (4.3%) with venous thrombosis. The 1-year cumulative incidence of thrombosis on DOACs was 10.8% (95% CI, 3.8 to 15.8). The median follow-up for the VTE cohort was 17.3 months (IQR, 6.2 to 39.4). In the VTE cohort, 15 patients (10.9%) had thrombotic events, including seven (5.1%) with arterial thrombosis and 10 (7.3%) with venous thrombosis. The 1-year cumulative incidence of recurrent thrombosis on DOACs was 11.7% (95% CI, 6.0 to 19.6). No significant difference in thrombosis incidence was observed between the AF and VTE cohorts (p=0.591) (Fig. 1B). Venous thrombosis outcomes occurred significantly more often in the VTE cohort than in the AF cohort, as shown in the S4 Fig. Although there was no association between MPN subtypes and overall thrombosis events, arterial thrombosis events were most common in the ET group, followed by the PV and MPN groups (Fig. 1C, S5 Fig.).
3. Incidence of bleeding
Seventeen patients (4.6%) were hospitalized for major bleeding events while on DOACs, including seven (1.9%) with ICH and 10 (2.7%) with hospitalization for GI bleeding. The 1-year cumulative incidence of hospitalized for major bleeding on DOACs was 3.7% (95% CI, 2.0 to 6.4) (Fig. 2A). There was no significant difference in bleeding incidence between the AF and VTE cohorts (p=0.539) (Fig. 2B). Bleeding outcomes were not related to MPN subtypes (Fig. 2C).
In the AF cohort, 13 patients (5.6%) were hospitalized for major bleeding events, including five (2.2%) with ICH and eight (3.5%) for GI bleeding. The 1-year cumulative incidence of hospitalization for major bleeding on DOACs was 4.3% (95% CI, 2.0 to 8.0). In the VTE cohort, four patients (2.9%) were hospitalized for major bleeding events, including two (1.5%) with ICH and two (1.5%) for GI bleeding. The 1-year cumulative incidence of hospitalization for major bleeding events on DOACs was 2.5% (95% CI, 0.7 to 6.5).
4. Risk factors for thrombosis and bleeding
In thrombosis events, CHA2DS2-VASc scores ≥ 3 (hazard ratio [HR], 3.48; 95% CI, 1.23 to 9.85; p=0.019), the use of concomitant antiplatelet agent (HR, 2.57; 95% CI, 1.35 to 4.88; p=0.004), and cytoreduction (HR, 2.20; 95% CI, 1.08 to 4.49; p=0.030) were statistically significant risk factors for thrombosis (Table 2). Both univariate and multivariate analyses revealed no significant risk factors associated with hospitalization for major bleeding (S6 Table).
This study represents the first investigation into thrombosis and bleeding in MPN patients using DOACs for AF or VTE in an East Asian population. Considering the ethnic differences in thrombosis and bleeding risks, which are influenced by genetic, environmental, and lifestyle factors, our research holds significant importance.
Among MPN patients, 63% used DOACs for AF and 37% for VTE. Several reasons might explain why the AF cohort was larger than the VTE cohort. First, AF is relatively common in MPN patients; one study found that 13.5% of patients with ET or PV had atrial arrhythmias, 97% of which were AF. This prevalence increases to 31% in patients aged 80 or older [19]. Second, DOACs are prescribed to AF patients not only for secondary but also for primary prevention of stroke. Third, there may be stronger clinical guidelines or more substantial evidence supporting the use of DOACs in AF compared to VTE. Although DOACs are recommended for treating PE and DVT among VTE cases, there is no clear evidence supporting their use in unusual site VTEs [20,21]. Unusual site thrombosis, accounting for about 10% of all VTE cases, occurs more frequently in MPN patients than in the general population [21-23]. In the current study, splanchnic vein thrombosis accounted for 16.8% of the VTE cohort.
During the median follow-up duration of 22.3 months, 12.2% and 4.6% of patients encountered thrombotic and major bleeding events, respectively. Due to differences in patient populations, study designs, data sources, various biases, and follow-up durations, it is challenging to directly compare our data with previous DOAC studies. While our study showed a somewhat higher rate of thrombotic events compared to the MPN-DOACs study [16], which reported a 7.2% recurrence of thrombosis and a 5.9% incidence of major hemorrhagic complications on DOACs, this apparent difference can be explained by several factors. Increasing age has consistently proven to be an independent predictor of future thrombotic events in MPN [6,24]. Cardiovascular risk factors were significantly and independently associated with an increased rate of total thrombosis in ET patients [25]. The patient cohort included in our study is characterized by an elderly population with a median age of 74 years and a high cardiovascular risk profile, as indicated by a median CHA2DS2-VASc score of 4. These characteristics suggest that our study population was older and had a more significant burden of cardiovascular risk factors compared to those in previous DOAC studies.
The GIMEMA (Gruppo Italiano Malattie Ematologiche dell’Adulto) study reported that among 494 patients with PV or ET treated for arterial or venous thrombosis, 33.6% experienced recurrent thrombosis, while 5.4% suffered major bleeding, with 18.2% receiving long-term VKA therapy [26]. Similarly, the European Leukemia Network (ELN) found that among 206 MPN patients with typical site VTE, approximately 70% of whom were on long-term VKA therapy, 21.8% experienced recurrent thrombosis, and 5.8% experienced major bleeding [27]. To date, no clinical studies have directly compared the efficacy and safety of DOACs versus VKAs in MPN patients. Although comparing retrospective studies has its limitations, the consistent findings of no significant increase in the risk of recurrent thrombosis or bleeding events support the potential efficacy of DOACs in this patient population.
Traditional risk factors for MPN-associated thrombosis include advanced age (> 60 years), sex, a history of thrombosis, leukocytosis, and the presence of the JAK2 V617F mutation [25]. The risk factors for thrombosis recurrence were age over 60 and a history of prior thrombosis, while the subtype of MPN does not predict recurrence [26-28]. How et al. [15] reported that significant risk factors for thrombosis while using DOACs included a history of previous thrombosis, specific DOACs (dabigatran or edoxaban), and age < 65. In the current study, CHA2DS2-VASc scores ≥ 3, concomitant use of antiplatelet agents, and cytoreduction therapy were identified as statistically significant risk factors for thrombosis on DOACs. While MPN subtype was not linked to overall thrombosis events, ET had the highest incidence of arterial thrombosis events, followed by PV and then MF (p=0.106).
Thrombosis recurrence risk can be reduced with antithrombotic therapy and/or cytoreduction. According to a systematic review of MPN patients with a history of VTE, a combination of anticoagulation and cytoreduction may offer the lowest recurrence risk [29]. However, most studies had a high risk of bias, and clinical and statistical heterogeneity led to inconsistent findings, warranting caution in interpretation. The observation that concomitant antiplatelet therapy and cytoreduction are significant risk factors for thrombotic events in patients using DOACs may be attributed to several underlying biases and mechanisms. Firstly, treatment-risk bias is a critical factor; patients with a higher baseline thrombotic risk are more likely to receive intensive treatment regimens, including both antiplatelet agents and cytoreductive therapy. For patients with AF who have a CHA2DS2-VASc score of 2 or greater, along with additional cardiovascular conditions, the simultaneous use of anticoagulants and antiplatelet agents may be required to reduce the risk of thromboembolism. This is particularly relevant for those who have undergone percutaneous coronary intervention for acute coronary syndrome or vascular intervention for peripheral artery disease [30]. For MPN patients with venous thrombosis who have a JAK2 mutation or cardiovascular risk factors, the use of both anticoagulation and aspirin together is recommended [31]. While this dual therapy approach may be necessary for some, it inherently increases the complexity of managing thrombotic risk, potentially leading to an increased incidence of thrombosis despite anticoagulation.
In the context of MPNs, cytoreduction is typically employed to lower elevated blood cell counts and mitigate thrombotic risk. However, the efficacy of cytoreduction in preventing recurrent thrombosis remains inconsistent across studies. In the GIMEMA cohort, cytoreduction halved the risk of thrombosis, but its effect was limited to first arterial thrombosis [26]. In contrast, in the ELN cohort, cytoreduction was not associated with a reduction in recurrent thrombosis [27]. This inconsistency may reflect variations in patient populations, the degree of cytoreduction achieved, and the underlying disease biology. Given the nature of observational studies, unmeasured confounding factors, such as disease characteristics, including JAK2 mutation status, erythrocytosis, and thrombocytosis, may have influenced the results. Additionally, patients receiving concomitant antiplatelet therapy or cytoreductive treatment might have different DOAC dose adjustments or levels of treatment adherence, which could impact thrombosis risk. Further prospective studies are needed to clarify the precise impact of these treatments on thrombosis risk in this patient population.
MPN patients are prone to bleeding. A variety of factors, including differences in study design, definition of bleeding, selection bias, recording bias, and discrepancies in follow-up time, contribute to the inconsistent reporting of the incidence and risk factors of bleeding in MPN. Wille et al. [32] reported a 5.7% incidence of major bleeding in MPN patients and found that the use of antiplatelet agents or anticoagulants was associated with bleeding outcomes, while age, sex, MPN subtype, and mutation status were not. Kaifie et al. [33] found that 8.2% of MPN patients experienced major bleeding, not linked to thrombocytosis, thrombocytopenia, or use of antiplatelet agents, VKAs, or DOACs, but rather to previous thromboembolic events, splenomegaly, and heparin administration. The MPN-DOACs study reported a 5.9% incidence of major bleeding in MPN patients, identifying the MF subtype and the use of dabigatran as significant risk factors for bleeding on DOACs [16]. In this study, 4.6% of patients were hospitalized for major bleeding events while on DOAC therapy, including 1.9% with ICH and 2.7% with GI bleeding. Although the number of bleeding events was low, necessitating cautious interpretation, no statistically significant risk factors for bleeding outcomes with DOAC use were identified.
This study has several limitations. First, erroneous coding could result in misclassification bias, especially in the absence of laboratory validation results in HIRA databases. Second, due to the retrospective observational nature of the study, only associations can be drawn, and causal relationships cannot be inferred. Third, although an incident case was defined through several steps, prevalent cases may be included in this study. Fourth, a limitation of analyzing data using claims records is the inability to access information on laboratory findings related to thrombosis and bleeding risk factors, such as leukocytosis, thrombocytosis, thrombocytopenia, mutation status, and underlying inherited thrombophilia. Fifth, it was not possible to verify adherence and compliance. In a real-world setting, adherence to DOACs might be lower, potentially leading to suboptimal anticoagulation and a higher risk of thrombotic events. Lastly, the current study did not use a known bleeding score, such as HAS-BLED (Hypertension, Abnormal renal and liver function, Stroke, Bleeding, Labile international normalized ratio, Elderly, Drugs, or alcohol), which has been validated for VKAs but not for DOACs [34]. According to previous studies on MPN patients with AF, HAS-BLED scores were poor predictors of bleeding outcomes [35]. There is no proven bleeding score system for DOAC use yet, but a suitable system is expected to be established in future studies.
To date, the optimal anticoagulant approach remains challenging in MPN. Despite the limitations, such as the retrospective nature of the analysis, and the short follow-up period, our findings show that DOACs were both effective and safe. Future directions would include prospective longitudinal studies to assess the long-term efficacy of DOACs in anticoagulated MPN patients.
Supplementary materials are available at Cancer Research and Treatment website (https://www.e-crt.org).
crt-2024-738_S1_Fig.pdf
crt-2024-738_S2_Table.pdf
crt-2024-738_S3_Table.pdf
crt-2024-738_S4_Fig.pdf
crt-2024-738_S5_Fig.pdf
crt-2024-738_S6_Table.pdf

Ethical Statement

This study was performed in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of Seoul National University Bundang Hospital. The need for informed consent from each patient was waived because the authors did not have access to identifiable information (IRB No: X-2212-798-901).

Author Contributions

Conceived and designed the analysis: Lee JY, Lee JH, Bang SM.

Collected the data: Lee JY, Lee JH.

Contributed data or analysis tools: Lee JY, Lee JH, Park W, Seo J, Kang M, Jung EH, Kim SA, Suh KJ, Kim JW (Ji-Won Kim), Kim SH, Lee JO, Kim JW (Jin Won Kim), Kim YJ, Lee KW, Kim JH, Bang SM.

Performed the analysis: Lee JY, Lee JH,

Wrote the paper: Lee JY, Bang SM.

Supervision: Bang SM.

Writing - review and editing: Lee JY, Lee JH, Park W, Seo J, Kang M, Jung EH, Kim SA, Suh KJ, Kim JW (Ji-Won Kim), Kim SH, Lee JO, Kim JW (Jin Won Kim), Kim YJ, Lee KW, Kim JH, Bang SM.

Conflict of Interest

Conflict of interest relevant to this article was not reported.

Funding

This research was supported by the Seoul National University Bundang Hospital Research Fund (02-2022-0037).

Fig. 1.
Cumulative incidence of thrombosis on direct oral anticoagulant in all myeloproliferative neoplasm patients (A), by indication (B), and by myeloproliferative neoplasm subtype (C). AF, atrial fibrillation; ET, essential thrombo cythemia; MF, primary myelofibrosis; PV, polycythemia vera; VTE, venous thromboembolism.
crt-2024-738f1.jpg
Fig. 2.
Cumulative incidence of bleeding on direct oral anticoagulant in all myeloproliferative neoplasm patients (A), by indication (B), and by myeloproliferative neoplasm subtype (C). AF, atrial fibrillation; ET, essential thrombo cythemia; MF, primary myelofibrosis; PV, polycythemia vera; VTE, venous thromboembolism.
crt-2024-738f2.jpg
Table 1.
Clinical features of the cohort, by DOAC indication
Total (n=368) AF (n=231) VTE (n=137) p-value
Age (yr), mean±SD 72.5±10.8 73.4±9.8 70.9±12.1 0.048
Age (yr), median (IQR) 74 (66-80) 75 (68-80) 73 (64-80)
Age group (yr)
 < 65 69 (18.8) 32 (13.9) 37 (27.0) 0.007
 65-74 121 (32.9) 79 (34.2) 42 (30.7)
 ≥ 75 178 (48.4) 120 (51.9) 58 (42.3)
Male/Female 196/172 (53.3/46.7) 136/95 (58.9/41.1) 60/77 (43.8/56.2) 0.005
MPN subtype
 ET 179 (48.6) 116 (50.2) 79 (34.2) 0.089
 PV 119 (32.3) 36 (15.6) 63 (46.0)
 MF 70 (19.0) 40 (29.2) 34 (24.8)
CHA2DS2-VASc score
 Mean±SD 3.8±1.9 4.1±1.8 3.4±2.1 0.001
 Median (IQR) 4 (3-5) 4 (3-5) 4 (2-5)
CHA2DS2-VASc score group (%)
 0-2 86 (23.4) 39 (16.9) 47 (34.3) < 0.001
 ≥ 3 282 (76.6) 192 (83.1) 90 (65.7)
Hypertension 288 (78.3) 198 (85.7) 92 (65.7) < 0.001
Diabetes mellitus 135 (36.7) 89 (38.5) 46 (33.6) 0.341
Dyslipidemia 240 (65.2) 154 (66.7) 86 (62.8) 0.449
Congestive heart failure 131 (35.6) 105 (45.5) 26 (19.0) < 0.001
Myocardial infarction 16 (4.3) 11 (4.8) 5 (3.6) 0.613
Peripheral arterial disease 43 (11.7) 24 (10.4) 19 (13.9) 0.315
Chronic obstructive pulmonary disease 70 (19.0) 37 (16.0) 33 (24.1) 0.057
Moderate-severe chronic renal disease 64 (17.4) 40 (17.3) 24 (17.5) 0.961
Antiplatelets 188 (51.1) 118 (51.1) 70 (51.1) 0.998
 Aspirin 164 (44.6) 103 (44.6) 61 (44.5) 0.991
 Clopidogrel 85 (23.1) 57 (24.7) 28 (20.4) 0.351
 Othersa) 19 (5.2) 9 (3.9) 10 (7.3) 0.154
Cytoreduction 292 (79.3) 184 (79.7) 108 (78.8) 0.851
 Hydroxyurea 239 (64.9) 152 (65.8) 87 (63.5) 0.655
 Anagrelide 101 (27.4) 72 (31.2) 29 (21.2) 0.038
 Ruxolitinib 45 (12.2) 21 (9.1) 24 (17.5) 0.017

Values are presented as number (%) unless otherwise indicated. AF, atrial fibrillation; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category (female); DOAC, direct oral anticoagulant; IQR, interquartile range; MPN, myeloproliferative neoplasm; SD, standard deviation; VTE, venous thromboembolism.

a) Other antiplatelet agents include cilostazol, ticagrelor, and abciximab.

Table 2.
Univariate analysis and multivariate analysis for thrombosis
Thrombosis, n (%)
 Univariate
 Multivariate
Yes (n=45) No (n=323) HR (95% CI) p-value HR (95% CI) p-value
Age (yr)
 < 75 22 (48.9) 168 (52.0) Ref 0.684 Ref 0.707
 ≥ 75 23 (51.1) 155 (48.0) 1.13 (0.63-2.01) 0.88 (0.44-1.74)
Sex
 Female 21 (46.7) 151 (46.7) Ref 0.867 Ref 0.351
 Male 24 (53.3) 172 (53.3) 1.05 (0.59-1.88) 1.36 (0.71-2.61)
MPN diagnosis
 PV 14 (31.1) 105 (32.5) Ref 0.475 Ref 0.512
 ET 25 (55.6) 154 (47.7) 1.15 (0.6-2.21) 1.00 (0.51-1.96) 0.999
 MF 6 (13.3) 64 (19.8) 0.67 (0.26-1.71) 0.59 (0.22-1.58) 0.296
CHA2DS2-VASc
 0-2 4 (8.9) 82 (25.4) Ref 0.041 Ref 0.019
 ≥ 3 41 (91.1) 241 (74.6) 2.91 (1.05-8.08) 3.48 (1.23-9.85)
DOAC drug
 Rivaroxaban 18 (40.0) 119 (36.8) Ref 0.290 Ref 0.335
 Apixaban 17 (37.8) 96 (29.7) 1.01 (0.52-1.95) 0.989 1.03 (0.49-2.13)
 Dabigatran 2 (4.4) 26 (8.0) 0.36 (0.09-1.50) 0.160 0.40 (0.07-1.74)
 Edoxaban 8 (17.8) 82 (25.4) 0.58 (0.25-1.31) 0.187 0.58 (0.25-1.33)
Concomitant antiplatelet agent
 No 25 (55.6) 229 (70.9) Ref 0.001 Ref 0.004
 Yes 20 (44.4) 94 (29.1) 2.76 (1.54-4.95) 2.57 (1.35-4.88)
Cytoreduction
 No 10 (22.2) 127 (39.3) Ref 0.022 Ref 0.030
 Yes 35 (77.8) 196 (60.7) 2.23 (1.13-4.43) 2.20 (1.80-4.49)

CHA2DS2-VASc, congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category (female); CI, confidence interval; DOAC, direct oral anticoagulant; ET, essential thrombocythemia; HR, hazard ratio; MF, primary myelofibrosis; MPN, myeloproliferative neoplasm; PV, polycythemia vera.

  • 1. Grinfeld J, Nangalia J, Baxter EJ, Wedge DC, Angelopoulos N, Cantrill R, et al. Classification and personalized prognosis in myeloproliferative neoplasms. N Engl J Med. 2018;379:1416–30. ArticlePubMedPMC
  • 2. Barbui T, Finazzi G, Falanga A. Myeloproliferative neoplasms and thrombosis. Blood. 2013;122:2176–84. ArticlePubMedPDF
  • 3. Kc D, Falchi L, Verstovsek S. The underappreciated risk of thrombosis and bleeding in patients with myelofibrosis: a review. Ann Hematol. 2017;96:1595–604. ArticlePubMedPMCPDF
  • 4. Hultcrantz M, Bjorkholm M, Dickman PW, Landgren O, Derolf AR, Kristinsson SY, et al. Risk for arterial and venous thrombosis in patients with myeloproliferative neoplasms: a population-based cohort study. Ann Intern Med. 2018;168:317–25. ArticlePubMedPMC
  • 5. Rungjirajittranon T, Owattanapanich W, Ungprasert P, Siritanaratkul N, Ruchutrakool T. A systematic review and meta-analysis of the prevalence of thrombosis and bleeding at diagnosis of Philadelphia-negative myeloproliferative neoplasms. BMC Cancer. 2019;19:184.ArticlePubMedPMCPDF
  • 6. Marchioli R, Finazzi G, Landolfi R, Kutti J, Gisslinger H, Patrono C, et al. Vascular and neoplastic risk in a large cohort of patients with polycythemia vera. J Clin Oncol. 2005;23:2224–32. ArticlePubMed
  • 7. Carobbio A, Finazzi G, Antonioli E, Guglielmelli P, Vannucchi AM, Delaini F, et al. Thrombocytosis and leukocytosis interaction in vascular complications of essential thrombocythemia. Blood. 2008;112:3135–7. ArticlePubMedPMCPDF
  • 8. Barbui T, Carobbio A, Cervantes F, Vannucchi AM, Guglielmelli P, Antonioli E, et al. Thrombosis in primary myelofibrosis: incidence and risk factors. Blood. 2010;115:778–82. ArticlePubMedPDF
  • 9. Barbui T, Carobbio A, Rumi E, Finazzi G, Gisslinger H, Rodeghiero F, et al. In contemporary patients with polycythemia vera, rates of thrombosis and risk factors delineate a new clinical epidemiology. Blood. 2014;124:3021–3. ArticlePubMedPDF
  • 10. Barbui T, Thiele J, Passamonti F, Rumi E, Boveri E, Ruggeri M, et al. Survival and disease progression in essential thrombocythemia are significantly influenced by accurate morphologic diagnosis: an international study. J Clin Oncol. 2011;29:3179–84. ArticlePubMed
  • 11. Patrono C, Rocca B, De Stefano V. Platelet activation and inhibition in polycythemia vera and essential thrombocythemia. Blood. 2013;121:1701–11. ArticlePubMedPDF
  • 12. Steffel J, Collins R, Antz M, Cornu P, Desteghe L, Haeusler KG, et al. 2021 European Heart Rhythm Association practical guide on the use of non-vitamin K antagonist oral anticoagulants in patients with atrial fibrillation. Europace. 2021;23:1612–76. PubMedPMC
  • 13. January CT, Wann LS, Calkins H, Chen LY, Cigarroa JE, Cleveland JC Jr, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines and the Heart Rhythm Society in collaboration with the Society of Thoracic Surgeons. Circulation. 2019;140:e125–51. ArticlePubMed
  • 14. Stevens SM, Woller SC, Kreuziger LB, Bounameaux H, Doerschug K, Geersing GJ, et al. Antithrombotic therapy for VTE disease: second update of the CHEST guideline and expert panel report. Chest. 2021;160:e545–608. PubMed
  • 15. How J, Story C, Ren S, Neuberg D, Rosovsky RP, Hobbs GS, et al. Practice patterns and outcomes of direct oral anticoagulant use in myeloproliferative neoplasm patients. Blood Cancer J. 2021;11:176.ArticlePubMedPMCPDF
  • 16. Barbui T, De Stefano V, Carobbio A, Iurlo A, Alvarez-Larran A, Cuevas B, et al. Direct oral anticoagulants for myeloproliferative neoplasms: results from an international study on 442 patients. Leukemia. 2021;35:2989–93. ArticlePubMedPMCPDF
  • 17. Kim DS. Introduction: health of the health care system in Korea. Soc Work Public Health. 2010;25:127–41. ArticlePubMed
  • 18. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137:263–72. ArticlePubMed
  • 19. Mahe K, Delluc A, Chauveau A, Castellant P, Mottier D, Dalbies F, et al. Incidence and impact of atrial arrhythmias on thrombotic events in MPNs. Ann Hematol. 2018;97:101–7. ArticlePubMedPDF
  • 20. van Es N, Coppens M, Schulman S, Middeldorp S, Buller HR. Direct oral anticoagulants compared with vitamin K antagonists for acute venous thromboembolism: evidence from phase 3 trials. Blood. 2014;124:1968–75. ArticlePubMedPDF
  • 21. Abbattista M, Capecchi M, Martinelli I. Treatment of unusual thrombotic manifestations. Blood. 2020;135:326–34. ArticlePubMedPDF
  • 22. Kiladjian JJ, Cervantes F, Leebeek FW, Marzac C, Cassinat B, Chevret S, et al. The impact of JAK2 and MPL mutations on diagnosis and prognosis of splanchnic vein thrombosis: a report on 241 cases. Blood. 2008;111:4922–9. ArticlePubMedPDF
  • 23. Patel RK, Lea NC, Heneghan MA, Westwood NB, Milojkovic D, Thanigaikumar M, et al. Prevalence of the activating JAK2 tyrosine kinase mutation V617F in the Budd-Chiari syndrome. Gastroenterology. 2006;130:2031–8. ArticlePubMed
  • 24. Carobbio A, Thiele J, Passamonti F, Rumi E, Ruggeri M, Rodeghiero F, et al. Risk factors for arterial and venous thrombosis in WHO-defined essential thrombocythemia: an international study of 891 patients. Blood. 2011;117:5857–9. ArticlePubMedPDF
  • 25. Barbui T, Finazzi G, Carobbio A, Thiele J, Passamonti F, Rumi E, et al. Development and validation of an International Prognostic Score of thrombosis in World Health Organization-essential thrombocythemia (IPSET-thrombosis). Blood. 2012;120:5128–33. ArticlePubMedPDF
  • 26. De Stefano V, Za T, Rossi E, Vannucchi AM, Ruggeri M, Elli E, et al. Recurrent thrombosis in patients with polycythemia vera and essential thrombocythemia: incidence, risk factors, and effect of treatments. Haematologica. 2008;93:372–80. ArticlePubMed
  • 27. De Stefano V, Ruggeri M, Cervantes F, Alvarez-Larran A, Iurlo A, Randi ML, et al. High rate of recurrent venous thromboembolism in patients with myeloproliferative neoplasms and effect of prophylaxis with vitamin K antagonists. Leukemia. 2016;30:2032–8. ArticlePubMedPDF
  • 28. Hernandez-Boluda JC, Arellano-Rodrigo E, Cervantes F, Alvarez-Larran A, Gomez M, Barba P, et al. Oral anticoagulation to prevent thrombosis recurrence in polycythemia vera and essential thrombocythemia. Ann Hematol. 2015;94:911–8. ArticlePubMedPDF
  • 29. Hamulyak EN, Daams JG, Leebeek FW, Biemond BJ, Te Boekhorst PA, Middeldorp S, et al. A systematic review of antithrombotic treatment of venous thromboembolism in patients with myeloproliferative neoplasms. Blood Adv. 2021;5:113–21. ArticlePubMedPMCPDF
  • 30. January CT, Wann LS, Calkins H, Chen LY, Cigarroa JE, Cleveland JC Jr, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2019;74:104–32. PubMed
  • 31. Tefferi A, Barbui T. Polycythemia vera and essential thrombocythemia: 2021 update on diagnosis, risk-stratification and management. Am J Hematol. 2020;95:1599–613. ArticlePubMedPDF
  • 32. Wille K, Huenerbein K, Jagenberg E, Sadjadian P, Becker T, Kolatzki V, et al. Bleeding complications in bcr-abl-negative myeloproliferative neoplasms (MPN): a retrospective single-center study of 829 MPN patients. Eur J Haematol. 2022;108:154–62. ArticlePubMedPDF
  • 33. Kaifie A, Kirschner M, Wolf D, Maintz C, Hanel M, Gattermann N, et al. Bleeding, thrombosis, and anticoagulation in myeloproliferative neoplasms (MPN): analysis from the German SAL-MPN-registry. J Hematol Oncol. 2016;9:18.PubMedPMC
  • 34. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user-friendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest. 2010;138:1093–100. ArticlePubMed
  • 35. Leiva O, Jenkins A, Rosovsky RP, Leaf RK, Goodarzi K, Hobbs G. Predictors of increased risk of adverse cardiovascular outcomes among patients with myeloproliferative neoplasms and atrial fibrillation. J Cardiol. 2023;81:260–7. ArticlePubMed

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    • Survey of Clinical Practice in Chronic Myeloproliferative Neoplasms in Croatia: A Study by the MPN Working Group Party of the Croatian Cooperative Group for Hematologic Diseases (KROHEM)
      Ivan Krecak, Marko Lucijanic, Rajko Kusec
      Journal of Clinical Medicine.2025; 14(5): 1524.     CrossRef

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      The Role of Direct Oral Anticoagulants in Managing Myeloproliferative Neoplasms Patients
      Cancer Res Treat. 2025;57(2):612-620.   Published online September 20, 2024
      DOI: https://doi.org/10.4143/crt.2024.738
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    The Role of Direct Oral Anticoagulants in Managing Myeloproliferative Neoplasms Patients
    Image Image
    Fig. 1. Cumulative incidence of thrombosis on direct oral anticoagulant in all myeloproliferative neoplasm patients (A), by indication (B), and by myeloproliferative neoplasm subtype (C). AF, atrial fibrillation; ET, essential thrombo cythemia; MF, primary myelofibrosis; PV, polycythemia vera; VTE, venous thromboembolism.
    Fig. 2. Cumulative incidence of bleeding on direct oral anticoagulant in all myeloproliferative neoplasm patients (A), by indication (B), and by myeloproliferative neoplasm subtype (C). AF, atrial fibrillation; ET, essential thrombo cythemia; MF, primary myelofibrosis; PV, polycythemia vera; VTE, venous thromboembolism.

    Fig. 1.

    Fig. 2.

    The Role of Direct Oral Anticoagulants in Managing Myeloproliferative Neoplasms Patients
    Total (n=368) AF (n=231) VTE (n=137) p-value
    Age (yr), mean±SD 72.5±10.8 73.4±9.8 70.9±12.1 0.048
    Age (yr), median (IQR) 74 (66-80) 75 (68-80) 73 (64-80)
    Age group (yr)
     < 65 69 (18.8) 32 (13.9) 37 (27.0) 0.007
     65-74 121 (32.9) 79 (34.2) 42 (30.7)
     ≥ 75 178 (48.4) 120 (51.9) 58 (42.3)
    Male/Female 196/172 (53.3/46.7) 136/95 (58.9/41.1) 60/77 (43.8/56.2) 0.005
    MPN subtype
     ET 179 (48.6) 116 (50.2) 79 (34.2) 0.089
     PV 119 (32.3) 36 (15.6) 63 (46.0)
     MF 70 (19.0) 40 (29.2) 34 (24.8)
    CHA2DS2-VASc score
     Mean±SD 3.8±1.9 4.1±1.8 3.4±2.1 0.001
     Median (IQR) 4 (3-5) 4 (3-5) 4 (2-5)
    CHA2DS2-VASc score group (%)
     0-2 86 (23.4) 39 (16.9) 47 (34.3) < 0.001
     ≥ 3 282 (76.6) 192 (83.1) 90 (65.7)
    Hypertension 288 (78.3) 198 (85.7) 92 (65.7) < 0.001
    Diabetes mellitus 135 (36.7) 89 (38.5) 46 (33.6) 0.341
    Dyslipidemia 240 (65.2) 154 (66.7) 86 (62.8) 0.449
    Congestive heart failure 131 (35.6) 105 (45.5) 26 (19.0) < 0.001
    Myocardial infarction 16 (4.3) 11 (4.8) 5 (3.6) 0.613
    Peripheral arterial disease 43 (11.7) 24 (10.4) 19 (13.9) 0.315
    Chronic obstructive pulmonary disease 70 (19.0) 37 (16.0) 33 (24.1) 0.057
    Moderate-severe chronic renal disease 64 (17.4) 40 (17.3) 24 (17.5) 0.961
    Antiplatelets 188 (51.1) 118 (51.1) 70 (51.1) 0.998
     Aspirin 164 (44.6) 103 (44.6) 61 (44.5) 0.991
     Clopidogrel 85 (23.1) 57 (24.7) 28 (20.4) 0.351
     Othersa) 19 (5.2) 9 (3.9) 10 (7.3) 0.154
    Cytoreduction 292 (79.3) 184 (79.7) 108 (78.8) 0.851
     Hydroxyurea 239 (64.9) 152 (65.8) 87 (63.5) 0.655
     Anagrelide 101 (27.4) 72 (31.2) 29 (21.2) 0.038
     Ruxolitinib 45 (12.2) 21 (9.1) 24 (17.5) 0.017
    Thrombosis, n (%)
    		 Univariate
    		 Multivariate
    Yes (n=45) No (n=323) HR (95% CI) p-value HR (95% CI) p-value
    Age (yr)
     < 75 22 (48.9) 168 (52.0) Ref 0.684 Ref 0.707
     ≥ 75 23 (51.1) 155 (48.0) 1.13 (0.63-2.01) 0.88 (0.44-1.74)
    Sex
     Female 21 (46.7) 151 (46.7) Ref 0.867 Ref 0.351
     Male 24 (53.3) 172 (53.3) 1.05 (0.59-1.88) 1.36 (0.71-2.61)
    MPN diagnosis
     PV 14 (31.1) 105 (32.5) Ref 0.475 Ref 0.512
     ET 25 (55.6) 154 (47.7) 1.15 (0.6-2.21) 1.00 (0.51-1.96) 0.999
     MF 6 (13.3) 64 (19.8) 0.67 (0.26-1.71) 0.59 (0.22-1.58) 0.296
    CHA2DS2-VASc
     0-2 4 (8.9) 82 (25.4) Ref 0.041 Ref 0.019
     ≥ 3 41 (91.1) 241 (74.6) 2.91 (1.05-8.08) 3.48 (1.23-9.85)
    DOAC drug
     Rivaroxaban 18 (40.0) 119 (36.8) Ref 0.290 Ref 0.335
     Apixaban 17 (37.8) 96 (29.7) 1.01 (0.52-1.95) 0.989 1.03 (0.49-2.13)
     Dabigatran 2 (4.4) 26 (8.0) 0.36 (0.09-1.50) 0.160 0.40 (0.07-1.74)
     Edoxaban 8 (17.8) 82 (25.4) 0.58 (0.25-1.31) 0.187 0.58 (0.25-1.33)
    Concomitant antiplatelet agent
     No 25 (55.6) 229 (70.9) Ref 0.001 Ref 0.004
     Yes 20 (44.4) 94 (29.1) 2.76 (1.54-4.95) 2.57 (1.35-4.88)
    Cytoreduction
     No 10 (22.2) 127 (39.3) Ref 0.022 Ref 0.030
     Yes 35 (77.8) 196 (60.7) 2.23 (1.13-4.43) 2.20 (1.80-4.49)
    Table 1. Clinical features of the cohort, by DOAC indication

    Values are presented as number (%) unless otherwise indicated. AF, atrial fibrillation; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category (female); DOAC, direct oral anticoagulant; IQR, interquartile range; MPN, myeloproliferative neoplasm; SD, standard deviation; VTE, venous thromboembolism.

    Other antiplatelet agents include cilostazol, ticagrelor, and abciximab.

    Table 2. Univariate analysis and multivariate analysis for thrombosis

    CHA2DS2-VASc, congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, prior stroke, transient ischemic attack, or thromboembolism, vascular disease, age 65-74 years, sex category (female); CI, confidence interval; DOAC, direct oral anticoagulant; ET, essential thrombocythemia; HR, hazard ratio; MF, primary myelofibrosis; MPN, myeloproliferative neoplasm; PV, polycythemia vera.

    Table 1.

    Table 2.

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